Impacts of Phytophthora ramorum Canker
and Other Agents in Sonoma County
Forests1
Tedmund J. Swiecki2 and Elizabeth A. Bernhardt2
Abstract
To study impacts of sudden oak death (SOD), a lethal bark canker disease caused by
Phytophthora ramorum, we established permanent plots in Sonoma County forest types at
risk of SOD. Baseline stand and tree health data were collected in 2001 and the plots were
reassessed in 2004. The 250 plots (0.02 ha each) were located at 11 study locations in stands
containing Quercus agrifolia, Q. kelloggii, or Lithocarpus densiflorus as the dominant
hardwood species. By 2004, P. ramorum canker symptoms developed at two locations that
lacked symptoms in 2001, leading to new tree mortality at one of these locations. Between
2001 and 2004, plot level incidence of P. ramorum canker increased from 29 to 40 percent of
plots containing L. densiflorus and from 2 to 10 percent in plots containing Q. kelloggii. Plots
with Q. agrifolia showed a slight drop in P. ramorum canker (from 9 to 7 percent of plots)
due to apparent symptom remission in trees at one location. Between 2001 and 2004, the
percentage of trees with P. ramorum canker symptoms increased at three of four locations
with symptomatic SOD canker hosts. Mortality due to both P. ramorum and other agents
increased at 9 of 11 study locations between 2001 and 2004. Among SOD canker hosts that
died during this period, mortality was due to P. ramorum in 4 of 16 Q. kelloggii, 7 of 18 Q.
agrifolia, and 18 of 50 L. densiflorus. In most study locations, annual background mortality
unrelated to P. ramorum was less than 1 percent per year between 2001 and 2004. Over this
same period, mortality due to P. ramorum exceeded background mortality at three locations
and equaled it at a fourth. At one L. densiflorus location, mortality associated with an
unidentified bark canker was comparable to levels of mortality associated with P. ramorum at
other locations. Only P. nemorosa and P. pseudosyringae were isolated at this location.
Keywords: California black oak, coast live oak, Lithocarpus, mortality, Quercus, SOD,
sudden oak death, tanoak.
Introduction
Phytophthora ramorum has become established in native forests in a number of
counties in Northern and Central California, including Sonoma County. Host trees
that can be killed by P. ramorum canker (sudden oak death or SOD), including
tanoak (Lithocarpus densiflorus), coast live oak (Quercus agrifolia), and California
black oak (Q. kelloggii), are important components of many Sonoma County forests
and woodlands. Elevated mortality of these SOD canker hosts due to P. ramorum
canker has the potential to severely impact many important forest ecosystems in
Sonoma and other counties.
In summer 2001, with funding provided by the Sonoma County Fish and
Wildlife Advisory Board, we established a set of permanent research/monitoring
1
Abbreviated version of this paper was presented at the Sixth California Oak Symposium: Today’s
Challenges, Tomorrow’s Opportunities, October 9-12, 2006, Rohnert Park, California.
2
Principal and Plant Pathologists, Phytosphere Research, 1027 Davis Street, Vacaville, CA 95687.
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GENERAL TECHNICAL REPORT PSW-GTR-217
plots in Sonoma County woodlands and forests at risk due to P. ramorum canker
(Swiecki and Bernhardt 2001). Primary objectives of this initial project were to
assess overall disease impacts in various forest types and establish baseline
conditions against which future changes could be measured. Targeted stands were
those with a major component of tanoak, coast live oak, and/or California black oak.
Once baseline conditions within plots had been established, subsequent
assessments of the plots were to be used to document the rate and pattern of disease
spread within stands and disease progress in individual trees. As part of a project
funded by the USDA-Forest Service, the plots established in 2001 were reevaluated
in the summer of 2004 (Swiecki and Bernhardt 2005). The objectives of this second
project were to estimate the overall impact of SOD on affected forest types and to
monitor the spread of disease over time. In this paper, we report on changes in
disease distribution, tree mortality, and overall tree health in these plots between
summer 2001 and summer 2004.
Methods
In the summer of 2001, we established 250 plots at eleven locations throughout
Sonoma County where tanoak, coast live oak, and/or California black oak were
common (table 1). Plots were circular with a radius of 8 m measured parallel to the
ground slope (plot area 0.02 ha=0.05 acre). Plots at each location were established at
vertices of a grid superimposed over a map of the location and are unbiased with
respect to tree condition or the presence or absence of disease. The only requirements
for establishing a plot at a grid intersection was that SOD canker host species (coast
live oak, California black oak, and/or tanoak) were present and the slope was
navigable (generally no greater than about 70 percent slope). The nominal spacing
between grid points was 50 m as plotted on a topographic map, with the exception of
the first location (Jack London SP), where the grid spacing was 60 m. Ground
distances between plot centers are generally greater than 50 m because of ground
slope. Because only plots containing SOD canker host were sampled, the pattern of
sampled plots often differs from the idealized sampling grid. The overall area
represented by the sampled plots in each grid varied from about 4.7 to 14 ha (table
1), depending on the distribution of the host trees at each location. The sampling plan
is described in detail in Swiecki and Bernhardt (2001).
We used a handheld GPS receiver (Garmin® GPS 76) with a high-gain external
Gilsson® GPS antenna mounted on a telescoping mast to geolocate the specified plot
vertices during plot establishment in 2001 and to relocate plots in 2004. One to
several trees in or near each plot were marked with numbered aluminum tree tags in
2001. We also recorded the distance and azimuth from tagged trees to each plot
center to permit precise relocation of plot centers.
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Impacts of Phytophthora ramorum Canker and Other Agents in Sonoma County Forests—Swiecki
Table 1—Study locations and numbers of plots, approximate areas, and host species present
at each.
Approximate
Number of
plot grid area1
SOD canker
Location
Abbreviation
plots
(ha)
host species
Jack London State
JLSP
24
8.2
Cal. black oak,
Park
tanoak, coast
live oak
Sugarloaf Ridge
SRSP
25
6.7
coast live oak
State Park
Lake Sonoma
LS
24
8.8
coast live oak,
(Army Corps of
Cal. black oak
Engineers)
Weston (private
Weston
26
7.2
coast live oak,
land)
Cal. black oak
Austin Creek State ACSRA
25
7.5
tanoak, Cal.
Recreation Area
black oak
Modini (private
Modini
25
14.0
Cal. black oak,
land)
coast live oak
Annadel State Park ASP
24
7.5
Cal. black oak
Salt Point State
SPSP
18
5.5
tanoak
Park
Helen Putnam
HPRP
24
5.3
coast live oak,
Regional Park
Cal. black oak
Foothill Regional
FRP
15
4.7
Cal. black oak,
Park
coast live oak
Sonoma Coast
SCSB
21
6.4
tanoak
State Beach
1
Plot grid areas were estimated by drawing an irregular polygon around the plots at each location using
ArcView® GIS software. Polygon edges were set approximately 30 m beyond plot centers.
Trees were included in plots if the edge of the main stem was within 8 m of the
plot center. A hand-held laser rangefinder (Leica® Disto Classic) was used to
determine which trees were within a plot. In each plot, we collected detailed disease
data on up to three tagged SOD canker host trees in or near each plot. These trees are
referred to as tally trees. Tally trees were sometimes located beyond the 8 m plot
boundary in plots that had few live SOD canker host trees. These out-of-plot tally
trees are considered only in calculations related to change in disease status and
disease on a percentage basis, but are excluded from plot-based density calculations.
All other SOD canker host trees in the plots were categorized with respect to
species, canopy position (overstory or understory) and disease status. We noted the
type and extent of P. ramorum canker symptoms present and whether the tree was in
decline or dead due to other agents. We also noted changes in the status of trees other
than canker hosts in the plots (for example, decline or mortality). Other plot data
evaluated included overall tree cover, California bay (Umbellularia californica)
cover, the presence of P. ramorum-like foliar symptoms on California bay, poison
oak (Toxicodendron diversilobum) cover, shrub species present, overall shrub cover,
canker host regeneration, and the presence of other disease agents in the plot.
In 2001, some suspected P. ramorum cankers were sampled for pathogen
isolation by Steven Swain (then with Sonoma County UC Cooperative Extension).
Most of those isolations were conducted in the late summer of 2001. In the 2004
resurvey, we conducted additional sampling for pathogen isolation, primarily to (1)
determine whether P. ramorum was present at locations where it had not been found
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GENERAL TECHNICAL REPORT PSW-GTR-217
previously, (2) clarify the infection status of trees in known P. ramorum-infested
areas that had ambiguous or atypical symptoms, or (3) determine whether other
Phytophthora spp., including P. nemorosa and/or P. pseudosyringae, were present at
locations with symptomatic trees. In particular, numerous symptomatic plants were
sampled at Austin Creek in 2004 to determine whether any of the cankers at this site
were caused by species other than P. ramorum.
Most isolations were made from stem cankers on SOD canker hosts or from
California bay leaves, but a few other host species were also sampled (table 2).
Tissue pieces from sampled plants were placed into PARP agar plates (Erwin and
Ribeiro 1996) to confirm the presence of P. ramorum or other Phytophthora species.
Plates were transported to the lab of Dr. David Rizzo at UC Davis for incubation and
identification of fungi that grew out on the PARP plates.
Data Management and Analysis
Data summaries and analyses were prepared using JMP® statistical software, version
5.1.2 (SAS Inc., Cary NC). We used the likelihood ratio chi square test to test for
independence of variables in two-by-two or larger contingency tables. We used
paired t-tests to test for mean differences in continuous variables recorded for
individual plots in 2001 and 2004. Unless otherwise indicated, effects or differences
are referred to as significant if p≤0.05.
Results
The densities of SOD canker hosts at each study location are shown in figure 1. A
total of 460 coast live oak, 373 California black oak, and 645 tanoak trees were
included in the study. Tally trees, for which the most detailed health data was
collected, included 229 coast live oaks, 251 California black oaks, and 180 tanoaks.
As shown in figure 1, California bay, an epidemiologically important foliar host of P.
ramorum, was present within plots at 7 of the 11 study locations.
1300
1200
Other trees
1100
QK
QA
LD
UC
Trees per ha
1000
900
800
700
600
500
400
300
200
100
0
SPSP
SCSB
ACSRA
JLSP
FRP
ASP
Modini
HPRP
SRSP
Weston
LS
Figure 1—Composition of forests at each study location in trees/hectare.
LD=Lithocarpus densiflorus; QA=Q. agrifolia; QK=Q. kelloggii; UC=Umbellularia
californica; Other trees=other oak, hardwood, and/or conifer species.
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Impacts of Phytophthora ramorum Canker and Other Agents in Sonoma County Forests—Swiecki
Presence of P. ramorum and Other Phytophthora Species at
Study Locations
At the time of the original 2001 survey, sampling conducted by members of David
Rizzo’s lab at the University of California, Davis, had confirmed the presence of P.
ramorum at three of the study locations: Jack London, Sugarloaf Ridge, and Austin
Creek. No additional locations had positive confirmations of P. ramorum as the result
of sampling of suspected P. ramorum cankers in 2001.
The results of the more extensive sampling conducted in 2004 are shown in
table 2. In 2004, P. ramorum was the only Phytophthora species isolated from stem
cankers or California bay foliage at the three locations (Austin Creek, Jack London,
and Sugarloaf Ridge) that were known to have P. ramorum in 2001.
Two locations, Annadel and Lake Sonoma, lacked P. ramorum symptoms in
2001 but were confirmed as having P. ramorum present in 2004. At Annadel, several
California black oak trees showed canker symptoms in 2004 typical of those caused
by P. ramorum, and isolations confirmed its presence in trees in three plots. P.
ramorum was also isolated from cankers on a coast live oak near a fourth plot. In
addition, many California bay trees showed typical symptoms of leaf infection by P.
ramorum, and P. ramorum was confirmed on California bay leaves from eight plots.
We recovered P. ramorum in 2004 from symptomatic California bay foliage
from trees located along a small stream between plots at Lake Sonoma. Foliar
symptoms in California bay were only observed in this portion of the Lake Sonoma
plot grid, and no symptomatic oaks were observed in 2004. We had noted two
California black oaks trees with atypical bleeding bark cankers near this area in 2001,
but these cankers had become inactive by 2004 and did not appear to be typical of
active or inactive P. ramorum cankers. Tissue sampled from one of these two trees in
2004 did not yield any Phytophthora spp.
Table 2—Number of positive Phytophthora isolations out of the total number of units sampled
in 2004 at various study locations. Sampling units were individual trees for stem cankers and
single trees or localized groups of trees or plants for the foliar symptoms. P. ramorum was the
only Phytophthora species present in positive isolations with the exception of the Sonoma
Coast samples, which yielded both P. pseudosyringae and P. nemorosa.
California
California
Coast
Coast
Douglasbay
black oak
live oak redwood
fir
Location
Tanoak
Salt Point
0/141
Sonoma Coast
3/42
0/7
Austin Creek
13/16
14/16
1/2
2/2
0/1
Jack London
1/1
0/1
Annadel
8/9
3/3
1/1
Helen Putnam
0/4
Sugarloaf Ridge 2/2
1/4
Weston
0/4
0/2
Lake Sonoma
1/2
0/1
1
2
An additional isolation from California huckleberry (Vaccinium ovatum) was also negative.
Leaves from one tree yielded P. pseudosyringae; leaves from two other trees yielded P. nemorosa.
Sonoma Coast was the third location where Phytophthora spp. was newly
isolated in 2004. P. nemorosa and P. pseudosyringae were isolated from leaves of
California bay, which is common at this location (fig. 1). However, P. ramorum was
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GENERAL TECHNICAL REPORT PSW-GTR-217
not isolated from California bay leaves or tanoak cankers sampled at this location
(table 2).
Bark cankers were present on about 20 percent of the tanoaks at Sonoma Coast
(fig. 2), but canker symptoms on tanoaks at this location were generally not typical of
those caused by P. ramorum. Many of the cankers that had recent bleeding in 2004
were small and did not appear to be very aggressive. Many cankers originally noted
in 2001 appeared inactive in 2004, with no recent bleeding, and some had callus
development at the old canker margin. In some trees, the bark was only affected to a
shallow depth. The phloem tissues in these shallow cankers subsequently decayed to
a light-colored, powdery consistency and eventually sloughed off, leaving a
somewhat eroded appearance to the bark surface.
No other likely causes of the bark cankers at Sonoma Coast were identified.
Other pathogens observed on tanoak at this location included Cryphonectria gyrosa,
which causes stem cankers but is readily recognized by its distinctive sporulation,
and the root pathogens Armillaria spp. and Inonotus dryadeus.
A small number of tanoaks at Salt Point had bark cankers similar to those seen
at Sonoma Coast (fig. 2). These included the non-aggressive shallow cankers that
decayed to form a light powdery material. We also observed numerous callused
cankers with exposed wood in the center, similar to canker rot cankers seen in some
oaks. None of the tanoak cankers sampled at this location yielded any Phytophthora
spp. No California bay trees are present within the plot grid for sampling.
Especially at Sonoma Coast, many trees with extensive cankers were
subsequently attacked by ambrosia beetles (Monarthrum spp.) and the sapwooddecaying fungus Hypoxylon thouarsianum (fig. 2). Tree mortality associated with
these stem cankers increased substantially at both Salt Point and Sonoma Coast
between 2001 and 2004.
Dead with bark
cankers
Bark cankers &
beetles & or H.
thouarsianum
Bark cankers
SPSP 01
SPSP 04
SCSB 01
SCSB 04
0%
5%
10%
15%
20%
25%
Percent of tanoaks with symptoms
Figure 2—Incidence of symptoms in tanoak associated with an unidentified bark
canker at Salt Point (SPSP) and Sonoma Coast (SCSB) in 2001 and 2004. Symptom
classes are analogous to the early, late, and dead classification system used for P.
ramorum canker (fig. 3).
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Impacts of Phytophthora ramorum Canker and Other Agents in Sonoma County Forests—Swiecki
Changes in P. ramorum Disease Levels
The proportion of trees with P. ramorum canker symptoms increased at the two
tanoak locations with known P. ramorum infestations, and in the new disease front at
Annadel (fig. 3). The increase in the proportion of symptomatic trees was most
dramatic at Austin Creek, nearly tripling since 2001. However, the proportion of
symptomatic trees at Sugarloaf Ridge actually declined slightly between 2001 and
2004 due to the apparent remission of canker symptoms in some trees. All four
locations showed an increase in the proportion of trees killed by P. ramorum (fig. 3).
Across the four locations shown in figure 3, the percentage of plots that had
trees with P. ramorum canker symptoms increased from 22 to 38 percent. The
percent of plots with P. ramorum canker symptoms on California black oak and
tanoak increased, but the percentage of plots with P. ramorum canker symptoms on
coast live oak decreased slightly between 2001 and 2004 (table 3). The slight drop in
the incidence of P. ramorum canker symptoms in coast live oak was due to apparent
symptom remission in two trees at Sugarloaf Ridge, which were the only
symptomatic trees in their respective plots.
ACSRA 01
ACSRA 04
JLSP 01
JLSP 04
ASP 01
ASP 04
% Dead
% Late
SRSP 01
% Early
SRSP 04
0%
5%
10%
15%
20%
25%
30%
35%
40%
45%
50%
55%
Percent of SOD canker hosts
Figure 3—Changes in P. ramorum symptom classes between 2001 and 2004 at
Austin Creek (ACSRA), Jack London (JLSP), Annadel (ASP), and Sugarloaf Ridge
(SRSP). Early = bleeding cankers only; Late = cankers and associated sporulation of
Hypoxylon thouarsianum and/or damage by wood boring beetles, primarily ambrosia
beetles (Monarthrum spp.); Dead = entire tree killed by P. ramorum canker.
Multistemmed trees with both live stems and stem(s) killed by P. ramorum were
classified as having late disease symptoms.
Table 3—Percent of plots with SOD symptoms on canker host species in 2001 and 2004.
Year
2001
2004
California black oak (119 plots)
2
10
coast live oak (114 plots)
9
7
tanoak (73 plots)
27
40
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GENERAL TECHNICAL REPORT PSW-GTR-217
In comparing the spatial distribution of disease in 2001 and 2004, it appeared
that disease distribution was relatively static at Jack London and Sugarloaf, and was
spreading from one or more disease loci within the plot grids at Annadel and Austin
Creek. At all four locations, symptoms on California bay were more widely
distributed than were P. ramorum cankers on the canker host species. Furthermore,
plots with P. ramorum canker were commonly adjacent within the plot grid to other
plots with symptomatic trees, especially in the 2004 evaluation. This pattern was
especially evident at Austin Creek. Between 2001 and 2004, disease appeared to
expand outward from areas that had infected trees in 2001 (fig. 4).
Figure 4—Distribution of P. ramorum symptoms in Austin Creek plots in 2001 (dark
bar to left of symbol) and 2004 (light bar to right of symbol). Bars indicate the number
of symptomatic SOD canker hosts, including trees in plots and additional tagged
trees beyond plot edges. The minimum bar height shown indicates one tree. Symbols
indicate plot locations. Plots containing California bay are denoted with circles; a
black dot in the center of the circle indicates that P. ramorum symptoms were present
on California bay foliage. Plots without California bay are denoted with triangles.
Mortality of SOD Canker Host Trees
Between 2001 and 2004, mortality increased among all SOD canker hosts (fig. 5) and
the percentage of plots with mortality also increased (table 4). Between the 2001 and
2004 evaluations, the number of dead California black oak trees more than doubled,
from 13 to 29, whereas coast live oak and tanoak showed smaller relative increases in
mortality. P. ramorum contributed to the increase in mortality between 2001 and
2004 in each species, accounting for 4 of 16 dead California black oaks, 7 of 18 dead
216
Impacts of Phytophthora ramorum Canker and Other Agents in Sonoma County Forests—Swiecki
coast live oaks, and 18 of 50 dead tanoaks. Among all mortality rated in 2004 (that is,
all trees estimated to have died after 1991), P. ramorum was responsible for 5 of 29
dead California black oaks, 12 of 41 dead coast live oaks, and 31 of 116 dead
tanoaks.
Mortality due to agents other than Phytophthora spp. was mostly due to wood
decay fungi. Important pathogens we observed on oaks and/or tanoaks in plots
included Inonotus andersonii, I. dryophilus, I. dryadeus, Ganoderma spp., Laetiporus
gilbertsonii, and Armillaria spp.
Table 4—Percent of plots with dead trees of SOD canker host species in 2001 and 2004.
Year
2001
2004
California black oak (114 plots)
10
20
coast live oak (119 plots)
18
25
tanoak (73 plots)
49
67
Levels of mortality due to both P. ramorum and other agents varied between
study locations. Tree mortality due to P. ramorum canker greatly exceeded mortality
due to other causes at both Austin Creek and Jack London (fig. 5). At Sugarloaf
Ridge, mortality due to P. ramorum canker approached, but was less than, mortality
due to other agents. At Annadel, where P. ramorum canker symptoms first appeared
in the 2004 evaluation, mortality due to other causes was still much more prevalent
than mortality due to P. ramorum.
The overall mortality percentages shown in figure 5 include trees rated in the
2001 survey as having died within the previous 10 years. Hence, the data for 2004
bars in these figures represent 13-year estimated mortality. In contrast, mortality
occurring between the 2001 and 2004 evaluations does not include uncertainties
associated with the year of mortality of trees that were dead in 2001. We used both
2001to 2004 observed mortality and the 1991 to 2001 estimated mortality rates to
calculate annual mortality rates for all locations (fig. 6).
Estimated annual background mortality rates for the 2001 to 2004 interval were
close to or somewhat higher than those for the 1991 to 2001 interval for most
locations. Two locations, Foothill and Helen Putnam, had no new mortality among
SOD canker hosts between 2001 and 2004. Overall, the background mortality rate
was about 1 percent or less per year for both time intervals at all locations. The
differences in background mortality rates between and within locations shown in
figure 6 were not significant. In all locations, some tree mortality was associated with
wood decay fungi, especially canker rot fungi such as I. andersonii and I. dryophilus,
and root disease fungi such as Ganoderma. This background mortality excludes
mortality due to P. ramorum canker and the unknown bark canker at Sonoma Coast
and Salt Point.
Annual P. ramorum mortality rates were higher for 2001 to 2004 than for
1991to 2001 at all four locations with P. ramorum canker (fig. 6). For these four
locations, the annual mortality due to P. ramorum canker for the period 2001 to 2004
(2.03 percent per year) was significantly greater than for 1991 to 2001 (0.42 percent
per year; likelihood ratio p=0.02). Furthermore, annual 2001 to 2004 mortality due to
P. ramorum exceeded background mortality during this period at Jack London,
Austin Creek, and Sugarloaf Ridge, and equaled it at Annadel (fig. 6).
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GENERAL TECHNICAL REPORT PSW-GTR-217
28%
26%
Mortality unrelated to P. ramorum
24%
2001
2004
Percent of trees
22%
20%
18%
16%
14%
12%
10%
8%
6%
4%
2%
0%
SPSP
SCSB
ACSRA
JLSP
FRP
ASP
Modini
HPRP
SRSP
Weston
LS
28%
26%
2001
2004
Mortality due to P. ramorum
24%
Percent of trees
22%
2001
20%
Mortality cause uncertain
18%
2004
16%
14%
12%
10%
8%
6%
4%
2%
0%
SPSP
SCSB
ACSRA
JLSP
FRP
ASP
Modini
HPRP
SRSP
Weston
LS
Figure 5—Cumulative mortality among SOD canker host trees due to P. ramorum
(bottom) and other causes (top) in 2001 and 2004 by location. Mortality in the 2001
survey includes trees rated as having died within the previous 10 years, i.e., mortality
since 1991. Total mortality in 2004 covers the period 1991 to 2004. Location
abbreviations are shown in table 1.
As shown in figure 6, recent (2001 to 2004) rates of mortality ascribed to the
unidentified bark canker at Sonoma Coast are similar to those due to P. ramorum at
Austin Creek. Sonoma Coast also had high levels of mortality in 2001 to 2004 that
could not be definitively assigned to a given cause (unknown bar in figure 6). If some
or most of this mortality is also related to the unidentified canker disease, it would
further increase the relative importance of this mortality category.
218
Impacts of Phytophthora ramorum Canker and Other Agents in Sonoma County Forests—Swiecki
Percent mortality per year 1991-2001
4.5%
4.0%
3.5%
P. ramorum canker
Other agents
Unknown
Other bark canker
3.0%
2.5%
2.0%
1.5%
1.0%
0.5%
0.0%
SPSP
SCSB ACSRA
JLSP
FRP
ASP
Modini
HPRP
SRSP Weston
LS
Percent mortality per year 2001-2004
4.5%
4.0%
3.5%
P. ramorum canker
Other agents
Unknown
Other bark canker
3.0%
2.5%
2.0%
1.5%
1.0%
0.5%
0.0%
SPSP
SCSB ACSRA JLSP
FRP
ASP
Modini
HPRP
SRSP Weston
LS
Figure 6—Annual mortality (percent mortality per year) of SOD canker host trees by
cause and study location for the periods 1991 to 2001 (top) and 2001 to 2004
(bottom). Location abbreviations are shown in table 1.
Discussion
Between 2001 and 2004, P. ramorum first appeared within our study areas at two
locations: Annadel and Lake Sonoma. Although P. ramorum was first confirmed at
Annadel SP on bay leaves in July 2003 (Allison Wickland, personal communication;
http://kellylab.berkeley.edu/OakMapper/viewer.htm), our isolations were the first
reports of P. ramorum on SOD canker hosts at this location. Based on the first known
appearance of symptoms in canker hosts, it appears that P. ramorum had been
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GENERAL TECHNICAL REPORT PSW-GTR-217
introduced into Annadel at a later point than it had been at Jack London and
Sugarloaf Ridge, two nearby state parks.
Based on its limited distribution, we believe that the observed infestation at
Lake Sonoma is also of relatively recent origin. The infested area is located along a
creek at the point where it is crossed by a constructed trail that is used by hikers,
equestrians, and bicyclists. An unpaved parking lot used primarily for horse trailer
parking and equestrian events is located adjacent to the creek upstream from the point
where the infestation was detected. It is likely that P. ramorum became established in
the creek area from infested materials (such as soil or foliage) that were transported
to the area by humans and introduced into the creek either via the trail or the parking
lot.
These findings suggest that even within counties or regions in which P.
ramorum is present, preventing transport of the pathogen material into apparently
non-infested areas may be an important method for reducing disease impacts. Current
regulatory programs at the state and federal level are directed at the prevention of
spread from infested counties to other counties or states. Within infested regions,
local programs to minimize or prevent intra-county and intra-regional pathogen
spread may be needed.
Increases in tree mortality were observed in all locations where P. ramorum was
found. Given the low rate of new infections at Sugarloaf Ridge and Jack London, it is
likely that annual P. ramorum mortality rates will decrease at these locations over the
next few years. In contrast, due to new infections at Austin Creek and Annadel,
annual P. ramorum-related mortality rates are likely to stay constant or increase over
the next few years.
Different stages of disease spread and progress were seen among the locations
with P. ramorum infestations. As of the 2004 assessment, Lake Sonoma appeared to
represent a site of very recent pathogen introduction; the pathogen had not yet
become widely established on California bay and canker hosts were not yet affected.
At Annadel, P. ramorum was more widely established in 2004, but the disease
epidemic in the plot area appeared to be at an early stage. P. ramorum had begun to
affect some canker hosts as well as California bay, but the epidemic was probably
still limited by inoculum production and distribution. At Austin Creek, the pathogen
was established in various parts of the plot grid by 2001, and disease progress among
the SOD canker hosts appeared to be at an exponential phase between 2001 and
2004. Jack London represents a later phase of the epidemic, in which the pathogen
had become well established throughout the plot grid. At this site, many of the trees
with the highest disease risk had already been infected by 2001, so the rate of new
infections was relatively low between 2001 and 2004.
These results suggest that disease progress among the SOD canker hosts in a
newly infested stand may follow a sigmoidal disease progress curve. The percentage
of newly-diseased trees probably increases slowly after the initial introduction of the
pathogen due to limited inoculum density. As the foliar disease epidemic spreads
throughout a stand, disease incidence in canker hosts can increase rapidly under
favorable conditions. As the number of uninfected susceptible hosts decreases, the
epidemic becomes limited by the lack of suitable hosts. The disease situation at
Sugarloaf Ridge may either represent this latter stage of the epidemic or a stalling of
the epidemic in the early phase due to environmental conditions that were relatively
unfavorable for disease development.
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Impacts of Phytophthora ramorum Canker and Other Agents in Sonoma County Forests—Swiecki
Inoculum production by P. ramorum is favored by late spring rainfall, although
levels and temporal patterns of inoculum production differ somewhat between mesic
tanoak stands and more xeric oak stands (Dave Rizzo, personal communication).
Based on our review of weather station data (Western Regional Climate Center
2006), most portions of Sonoma County had average to below average rainfall
without high amounts of late spring rain between our 2001 and 2004 evaluations.
Disease spread under these conditions may have been relatively low compared with
what would be expected under more favorable conditions, such as those that occurred
in spring 2005 and 2006. Informal observations indicate that disease levels have
increased dramatically in portions of Sonoma County since 2004. Reassessment of
these plots in 2007 would allow us to compare disease progress during periods with
different levels of inoculum production.
P. ramorum, P. nemorosa, and P. pseudosyringae were only confirmed at
locations that also had substantial amounts of California bay within the plots (fig. 1).
Previous research has shown a strong epidemiological link between California bay
proximity and coast live oak infection rates by P. ramorum (Swiecki and Bernhardt
2002). The presence of other foliar hosts, with the possible exception of poison oak
(Swiecki and Bernhardt 2003), has not been correlated with infection of California
black oak or coast live oak. Futhermore, P. ramorum does not normally sporulate on
infected bark cankers of its oak hosts (Davidson and others 2005). Hence, California
black oaks and coast live oaks at the Helen Putnam, Modini, and Foothill study
locations and much of the Weston location may be very unlikely to develop P.
ramorum canker under current stand conditions. Disease risk at sites containing
tanoak is not completely related to California bay presence since tanoak sustains
foliar and twig infections that can produce P. ramorum inoculum (Rizzo and others
2002). Therefore, tanoak stands in Sonoma County are likely to be at risk from P.
ramorum for the foreseeable future.
The cause of the bark canker symptoms seen at Sonoma Coast and Salt Point
remains uncertain. P. nemorosa and P. pseudosyringae were isolated from bay leaves
in the plots at Sonoma Coast, but we were unable to recover any Phytophthora spp.
from active bleeding cankers at either location. However, given the relatively low
numbers of isolations performed, we cannot rule out P. nemorosa and/or P.
pseudosyringae as possible causes of the cankers. P. ramorum also cannot be entirely
ruled out as a possibility at this point. However, the fact that P. ramorum was not
recovered from symptomatic trees in either 2001 or 2004 strongly suggests that this
species was either not present or was not associated with the sampled cankers.
P. nemorosa and P. pseudosyringae are recently-described species (Hansen and
others 2003, Jung and others 2003) and further analysis is needed to determine how
long these species have been present in California forests. If most of the cankers at
Sonoma Coast are actually caused by one or both of these species, it would imply
that these agents may have impacts comparable to P. ramorum in at least some
locations. The greater importance of this canker disease at Sonoma Coast relative to
Salt Point may be related to the fact that California bay, which is also a host of P.
nemorosa and P. pseudosyringae, is common at Sonoma Coast but absent at the Salt
Point study location (fig. 1).
221
GENERAL TECHNICAL REPORT PSW-GTR-217
Acknowledgements
The research reported here was funded by USDA Forest Service (Agreement
CF1052021-130) through UC agreement K007582-01 with Dr. David Rizzo,
Department of Plant Pathology, University of California, Davis. We thank Dr. Rizzo
for his cooperation and support during this project. The original establishment of the
Sonoma County plots was funded through a grant from the Sonoma County Fish and
Wildlife Advisory Board. We thank John Westoby, former Sonoma County
Agricultural Commissioner, for his efforts to secure the initial funding to establish
the plots.
We thank the following people for assistance with fieldwork and pathogen
isolations: Djibo Zanzot, John Bienapfl; Elizabeth Fitchner, Allison Wickland,
Steven Swain, and Frances Swiecki-Bernhardt. We also thank California State Parks,
U.S. Army Corps of Engineers, Sonoma County Agricultural Preservation and Open
Space District, Sonoma County Regional Parks, and the private landowners who
provided permissions and access to the locations used for these studies.
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Continued
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